1. Technical Field
This document relates to methods and materials for reducing ischemia-reperfusion injury. For example, this document relates to administering abscisic acid to reduce tissue injury caused by reperfusion following ischemia.
2. Background Information
Ischemia is a restriction in blood supply to tissues, which causes a shortage of elements needed for the tissues to survive such as oxygen and glucose. Surprisingly, the restoration of the physiological blood flow (e.g., reperfusion) causes further tissue lesions in many cases. See, e.g., Hausenloy and Yellon, J. Clin. Invest., 123(1):92-100 (2013). An excessive inflammatory response is believed to play an essential role in the pathogenesis of this ischemia-reperfusion injury. For example, during the reperfusion of ischemic tissue, the primary tissue lesions are the consequences of an overproduction of reactive oxygen species that can result in oxidative damage such as lipid peroxidation, protein oxidation, and DNA damage. In some cases, this leads to the initiation of cell death (e.g., apoptosis or necrosis). Furthermore, reactive oxygen species can activate certain downstream signaling pathways that up-regulate the expression of genes encoding pro-inflammatory proteins.
These local and systemic inflammatory responses caused by reperfusion following ischemia can lead to clinical symptoms and pathologies like lung failure (e.g., acute respiratory distress syndrome (ARDS)), renal insufficiency, cardiac arrhythmias, and skeletal muscle revascularization oedema. These clinical complications can significantly worsen the survival chances of patients. Thus, ischemia-reperfusion injury is an existing serious condition in the aftermath of many diseases and traumatic injuries.